It is a common clinical symptom caused by the stimulation of pain receptors in intracranial and external pain-sensitive structures. It is caused by the pain transmission pathway reaching the cerebral cortex. It is located in the upper half of the skull, including the eyebrow arch, the upper edge of the helix and the external occipital protuberance. Pain above the line

primary pain

secondary pain

Mechanical, chemical, biological stimulation, biochemical changes in the body

Primary pain, a common clinical condition, is a common chronic neurovascular disease with a prevalence rate of 5% to 10%.

feature

internal cause

external factors

unclear

vascular theory

neurological theory

trigeminal neurovascular theory

Retino-thalamic-cortical mechanism

other

Epidemiology

Types

Migraine possible

Cyclic disorders associated with migraines

Diagnostic criteria for migraine without aura

Diagnostic criteria for migraine with aura

Diagnostic criteria for chronic migraine

Common primary headache identification chart

Purpose

non-pharmacological treatment

medical treatement

The prognosis for most migraine patients is good

Migraine symptoms may gradually improve with age

Some patients can no longer have migraine attacks at the age of 60 to 70 years old

174 Chapter 8 Headache [Diagnosis and treatment of headaches] A detailed medical history can provide first-hand information for the diagnosis of headache. When collecting medical history, focus should be placed on asking about the onset and onset of headache. Frequency, onset time, duration, headache location, nature, pain level and accompanying symptoms; pay attention to asking about headache triggers and prodrome factors that aggravate and alleviate symptoms and headaches. In addition, a comprehensive understanding of the patient's age and gender, sleep and occupational status, past medical history, and concomitant The influence of general conditions such as disease, trauma history, medication history, poisoning history and family history on the onset of headache. In the diagnosis process of headache, the first thing to consider is First distinguish whether it is primary or secondary. The diagnosis of any primary headache should be based on the exclusion of secondary headaches. Comprehensive and detailed A thorough physical examination, especially an examination of the nervous system, head, face, and facial features, can help discover the location of the headache. Choose God appropriately and at the right time Auxiliary examinations such as imaging or lumbar puncture of cerebrospinal fluid can provide objective evidence for organic lesions in the face. The principles of prevention and treatment of headache include etiological treatment, symptomatic treatment and preventive treatment. In cases with a clear cause, the cause should be removed as soon as possible, such as facial Internal infections should be treated with anti-infectives. Those with intrafacial hypertension should dehydrate to reduce facial pressure. Tumors in the facial area need surgical removal. The cause cannot be corrected immediately For secondary headaches and acute attacks of various primary headaches, symptomatic treatment such as analgesia can be given to terminate or reduce headache symptoms, and at the same time, Headaches accompanied by symptoms such as dizziness and vomiting should be treated appropriately. People with recurring chronic headaches should take appropriate preventive measures Treatment to prevent frequent headaches. Migraine Chapter 1 Migraine is a common clinical primary headache, which is characterized by episodic, mostly hemilateral, moderate to severe, and pulsating headaches. It usually lasts 4 to 72 hours and may be accompanied by nausea and vomiting. Sound and light stimulation or daily activities can aggravate the headache. It can be relieved by being in a quiet environment and resting. Relieve headaches. Migraine is a common chronic neurovascular disease with a prevalence rate of 5% to 10%. 【Cause】 The cause of migraines is unknown, but may be related to the following factors: 1. Internal factors. Migraine has a genetic susceptibility. About 60% of migraine patients have a family history. The risk of migraine in their relatives is 3 to 6 times that of the general population. Familial hemiplegic migraine (FHM) is a common disease with high penetrance. Chromosome dominant inheritance is divided into three categories according to the mutant gene FHM. The mutant genes are CAC NA 1 A gene, ATP 1 A 2 gene and SCN 1 A gene. In addition, mutations in genes related to nervous system excitability are associated with common types of migraine, suggesting that migraine is associated with major Related to excitatory hormone disorder in brain nerve cells. This disease is more common in women than in men, and usually occurs in adolescence. It is easy to occur during menstruation, and may occur during pregnancy or postpartum period. Postmenstrual seizures decrease or stop. This suggests that endocrine and metabolic factors are involved in the pathogenesis of migraine. 2. External factors and environmental factors are also involved in the onset of migraine. Migraine attacks can be triggered by certain foods and medications. food included Cheese containing tyramine, meat and preserved foods containing nitrite, chocolate containing phenylethylamine, food additives containing monosodium glutamate and grapes Alcohol, etc.: Medications include oral contraceptives and vasodilators such as nitroglycerin. In addition, strong light, overwork, stress and relaxation after stress, Too much or too little sleep, fasting, stress, emotional instability, etc. are also triggering factors for migraines. 【Pathogenesis】 The pathogenesis of migraine is not very clear yet. Currently, there are mainly the following theories: 1. Vascular theory This theory believes that migraine is a primary vascular disease, caused by vasomotor dysfunction. intrafacial vasoconstriction Causes migraine aura symptoms, followed by dilation of blood vessels outside and inside the face, leading to pulsating headaches. carotid artery compression, vasoconstrictor Angular alkaloids such as ergotamine may relieve headaches supporting this theory. However, multiple recent imaging studies including air CT cerebral blood flow imaging SPEC T, PET and fMRI have confirmed that vasodilation does not necessarily exist during a migraine attack. It is currently believed that vasodilation is just a migraine headache An accompanying phenomenon rather than a necessary condition 2. Neurological theory This theory believes that migraine is a primary neurological disorder. Migraine aura is caused by cortical extension Caused by cortical spreading depressing (CSD). CSD refers to a disease that originates in the posterior cortex of the brain caused by various harmful stimuli. (Occipital lobe) nerve electrical activity inhibition zone, this inhibition zone expands to the adjacent cortex at a speed of 2 to 5 mm/min, accompanied by the occurrence of extended blood The amount is reduced (spreading o lig emi a); both do not expand according to the distribution of cerebral arteries, but according to the architectural pattern of cerebral cortex cells, moving forward Extension generally does not extend beyond the central sulcus. CSD can well explain migraine aura symptoms. In addition, the 5-hydroxytryptamine (5-HT)ergic neuron family

Chapter 8 Headache 175 Widely distributed in the brain, many effective antimigraine drugs act as central 5-HT receptor agonists or partial agonists, which suggests It shows that neuronal dysfunction is involved in the attack process of migraine. The ophthalmic branch of the cranial nerve enters the human trigeminal ganglion, or the posterior roots of the 1st and 2nd cervical nerves (C, C) to the C and C spinal ganglia, and then sends out nerve fibers. To the trigeminovascular complex (trig emi no vascular complex), nerve fibers are sent out after replacement, cross the brainstem and project to the thalamus. When the trigeminal ganglion and its fibers are stimulated, it can cause substance P and calcitonin gene-related peptide (calc it on in gene-related peptide). Increased release of C GRP) and other neuropeptides. These active substances act on the walls of adjacent cerebral blood vessels, causing blood vessels to dilate and cause pulsatility. Headache can also increase the permeability of blood vessels, leak out plasma proteins, produce aseptic inflammation, stimulate the transmission of pain fibers to the central nervous system, and form a vicious cycle. ring. Studies have shown that triptan preparations, HT receptor agonists, can act on the trigeminal neurovascular complex and the retroventral interior of the thalamus. 5-HT receptors in the lateral nucleus can terminate acute attacks of migraine; micro-infiltration of C GRP receptor antagonists into the human trigeminal neurovascular complex can effectively inhibit Inhibits the transmission of pain information in the trigeminal neurovascular system. It is suggested that neurofunctional hormone disorders in the trigeminal neurovascular complex and thalamus are also involved in migraine. The onset of pain. 4. Retino-thalamic-cortical mechanism Migraine is a disease related to dysregulation of sensory patterns, such as in patients with migraine before the attack Later, they are sensitive to light, sound, touch and touch. Recently, studies of migraine in blind people have found a link from retinal ganglion cells to the posterior thalamus. Activation of non-image-forming visual pathways may be one of the mechanisms by which light modulates migraine [Clinical manifestations] 052(2- Migraine mostly occurs in children and adolescence, reaching its peak incidence in young and middle-aged people. It is more common in women, and the ratio of male to female patients is about 1:2 to 1:3. ③ There is often a genetic background. The ICH D-3 migraine classification is shown in Table 8-2 Table 8-2 International Headache Society Migraine Classification Migraine without aura Migraine with aura 2.1 Migraine with typical aura 2.1.1 typical aura with headache 2.1.2 typical aura without headache 2.2 Migraine with brainstem aura 2.3 Hemiplegic migraine familial hemiplegic migraine 2.3.1 2.3.2 sporadic hemiplegic migraine 2.4 retinal migraine chronic migraine Complications of migraine status migraine us 4.1 persistent aura without infarction 4.2 4.3 Migraine cerebral infarction Migraine aura-triggered seizure 4.4 5 probable migraine 5.1 probable migraine without aura 5.2 Possible migraine with aura episodic syndromes that may be associated with migraine Recurrent gastrointestinal disturbance 6.1 cyclical vomiting syndrome 6.1.1 Abdominal migraine 6.1.2 benign paroxysm al vertigo 6.2 6.3 Benign paroxysmal torticollis (benign paroxysm al to rti coll is)

①Headache 176 Chapter 8 Head pain residence The following introduces the clinical manifestations of the main types of migraine: 1. Migraine without aura is the most common type of migraine, accounting for about 80%. The clinical manifestations are Recurrent pain on one or both sides of the forehead is pulsating, and when the pain persists, it can be complicated by contraction of the neck muscles. often accompanied by evil Symptoms include palpitations, vomiting, photophobia, phonophobia, sweating, general malaise, and scalp tenderness. This type of attack has a high frequency and can seriously affect the patient's work and life. Live life often requires frequent use of analgesics, which is prone to the emergence of a new type of headache - medication overuse headache (medic at i or overuse headache, MOH). This type of migraine is often closely related to menstruation. 2. Migraine with aura, accounting for about 10% of migraine patients. It may occur hours to days before the attack Prodromal symptoms include tiredness, inattention, and yawning. Reversible focal neurological symptoms often precede or occur during headache Symptoms are auras, manifested as visual, sensory, speech and motor defects or irritation symptoms. The most common are visual auras, such as blurred vision, dark spots, Flashes of light, bright spots, bright lines, or visual distortion; followed by sensory auras, verbal and motor auras are rare. Aura symptoms usually appear within 5 to 20 minutes. It develops gradually and lasts no more than 60 minutes; different signs may appear one after another. The headache occurs at the same time as the aura or within 60 minutes after the aura. Presently, pulsating headache on one or both sides of the forehead or behind the frame, often accompanied by nausea, vomiting, photophobia or phonophobia, paleness or sweating, polyuria, and irritability. Provocation, horrible smell and fatigue, etc. Headaches can be worsened by activity and relieved by sleep. The headache can last from 4 to 72 hours and subsides Fatigue, tiredness, irritability, weakness and poor appetite are common, and usually get better after 1 to 2 days mouth (1) Migraine with typical aura: It is the most common type of migraine with aura, and the aura manifests as complete Reversible visual, sensory, or speech symptoms without physical weakness. Occurrence at the same time as the aura or within 60 minutes after the aura is consistent with the characteristics of migraine The symptom of headache is a typical aura accompanied by headache. When a headache does not occur within 60 minutes after an aura, it is called a typical aura without headache. (2) Brainstem migraine with aura (basil ar-type migraine): It was also called basilar migraine in the past. The aura symptoms obviously originate from the brainstem. Clinically, dysarthria, tinnitus, hearing loss, diplopia, simultaneous visual symptoms in the nasal and topical fields of both eyes, ataxia, There was disturbance of consciousness and sensory abnormalities on both sides, but no symptoms of motor weakness. The occurrence of migraine at the same time as the aura or within 60 minutes of the aura Headache with painful characteristics, often accompanied by nausea and vomiting. (3) Hemiplegic migraine: rare in clinical practice. In addition to symptoms of motor weakness, the aura should also include visual One of three auras: consciousness, sensation and speech. Aura symptoms last from 5 minutes to 24 hours. Symptoms are completely reversible. At the same time or 60 Headache with characteristics of migraine occurs within minutes. For example, at least one first- or second-degree relative of a patient with hemiplegic migraine has Migraine aura that includes motor weakness is called familial hemiplegic migraine; if it is absent, it is called sporadic hemiplegic migraine. (4) Retinal migraine: Recurrent, fully reversible monocular visual impairment, including flickers and dark spots. or blindness accompanied by migraine attacks, with normal eye examinations between attacks. Similar to basilar migraine, visual aura symptoms often involve both eyes. Meanwhile, retinal migraine visual symptoms are limited to one eye and lack symptoms of nerve loss or irritation originating from the brainstem or cerebral hemisphere. 3. Chronic migraine, migraine attacks for more than 15 days per month for 3 consecutive months or more If there are at least 8 headache days per month with characteristics of migraine headaches, and headaches caused by drug overdose are excluded, chronic migraine can be considered. Headache. 4. Migraine complications (1) Status migraine us (status migraine us): migraine attacks last for ≥72 hours, and the pain is severe, However, there may be a short period of relief due to sleep or drug use. (2) Persistent aura without infarction: refers to patients with migraine with aura having one aura or multiple aura symptoms lasting for 1 period in one attack. More than 1 week old, most of them are bilateral; other symptoms of this attack are similar to previous attacks; neuroimaging is required to rule out cerebral infarction. (3) Migraine cerebral infarction: In rare cases, ischemic infarction in the corresponding blood supply area occurs after migraine aura symptoms. This aura symptom often lasts for more than 60 minutes, and the ischemic infarction focus is confirmed by neuroimaging, which is called migraine cerebral infarction. (4) Migraine aura-induced illness attacks: In rare cases, migraine aura symptoms can trigger illness attacks, and the onset of illness attacks Occurs during or within 1 hour after aura symptoms. 5. Children's periodic syndrome, which is often the prodromal of migraine, can be regarded as migraine isotopia. Clinically, periodic vomiting and recurrent episodes can be seen. Abdominal pain accompanied by nausea and vomiting is abdominal migraine and benign childhood paroxysmal dizziness. The attack is not accompanied by headache. As time goes by, Migraines may occur.

177 Chapter 8 Headache Migraine, with or without actinization 【diagnosis】 A clinical diagnosis is usually made based on the type of migraine attack, family history, and neurological examination. Brain CT, CTA, MRI, MR A Examination can rule out intrafacial organic diseases such as cerebrovascular disease, intrafacial aneurysms, and space-occupying lesions. The following introduces ICH D-3 migraine diagnosis Breaking standard. 1. Diagnostic criteria for migraine without aura (1) At least 5 attacks that meet the characteristics of (2) to (4). (2) Headache lasts for 4 to 72 hours (without treatment or treatment is ineffective). (3) Have at least 2 of the following headache characteristics: ① Unilateral; ② Pulsating; ③ Moderate or severe headache; ④ Daily activities (such as walking) or walking up stairs) can aggravate the headache, or actively avoid such activities when you have a headache. (4) The headache process is accompanied by at least one of the following: ① nausea and/or vomiting; ② photophobia and phonophobia. (5) Cannot be attributed to other diseases 2. Diagnostic criteria for migraine with aura (1) At least 2 attacks that meet the characteristics of (2) to (4). (2) At least one of the following completely reversible aura symptoms occurs: ①Visual symptoms, including positive manifestations (such as flashes, bright spots or bright lines) and/or negative manifestations (such as visual field defect); ② sensory abnormalities, including positive manifestations (such as pinprick sensation) and/or negative manifestations (such as numbness); ③Speech and/or language dysfunction; ④Motor symptoms, 5 brainstem symptoms, and retinal symptoms. (3) At least 2 of the following are met: ① At least 1 aura symptom gradually develops for ≥5 minutes, and/or at least 2 aura symptoms Continuous occurrence; ② Each aura symptom lasts for 5 to 60 minutes; ③ At least 1 aura symptom is unilateral; ④ Headache occurs with aura, or Occurs after an aura, less than 60 minutes apart (4) It cannot be attributed to other diseases and transient ischemic attack is excluded. 3. Diagnostic criteria for chronic migraine (1) Headache (tension-type headache or migraine) ≥15 days per month, lasting for more than 3 months, and meeting criteria (2) and (3) (2) The patient has at least 5 attacks that meet the criteria (2) to (4) for migraine without aura and/or the diagnostic criteria for migraine with aura. (2) and (3) (3) Headache lasts for more than 3 months, occurs for ≥8 days per month and meets any one of the following: ① Migraine without aura criteria (3) and (4); ②Diagnostic criteria for migraine with aura (2) and 3) (4) Cannot be attributed to other diseases 【Differential Diagnosis】 It is a rare episode of severe pain around one side of the eye that lasts for 15 minutes. 1. Cluster headache Minutes to 3 hours, attacks range from once every other day to 8 times a day. This disease is characterized by repeated and intensive attacks, but the headache is always unilateral and often accompanied by There are ipsilateral conjunctival congestion, tearing, runny nose, sweating on the forehead and face, and Horner's sign. The pain is often persistent, rarely accompanied by nausea and vomiting, and some cases may also present with paroxysmal and pulsating headaches. More common in young and middle-aged women Sexual, mood disorders, or psychological factors can worsen headache symptoms 3. Symptomatic migraine, a headache caused by vascular lesions in the head and neck, such as ischemic cerebrovascular disease disease, intracerebral hemorrhage, unruptured saccular aneurysms, and arteriovenous malformations; headaches due to nonvascular intraocular diseases such as intrafacial tumors; Headaches caused by internal infections such as brain swelling, meningitis, etc. These secondary headaches may also present clinically as migraine-like headaches, which may Accompanied by nausea and vomiting, but no typical migraine attack process, most cases have focal neurological deficit or irritation symptoms, facial and brain imaging Medical examination can reveal lesions. Headaches due to internal environmental disorders, such as hypertensive crisis, hypertensive encephalopathy, sub-disease or aura sub-disease, may manifest as It is a bilateral pulsating headache. The time of occurrence of headache is closely related to the increase in blood pressure. In some cases, neuroimaging examination may show reversibility. Manifestations of white matter damage. 4. Medication overuse headache is a secondary headache. The occurrence of headaches is related to the overuse of drugs, and may be migraine-like or Mixed headache with characteristics of both migraine and tension-type headache. The headache resolves or returns to its original state within 2 months after stopping the medication.

178 Chapter 8 Headache headache pattern. Medication overuse headache is not responsive to preventive treatment measures. 【treat】 C The purpose of migraine treatment is to reduce or terminate headache attacks, relieve accompanying symptoms, and prevent headache recurrence. Treatment includes medications and Two aspects of non-drug treatment. Non-drug treatment mainly focuses on strengthening publicity and education to help patients establish scientific and correct prevention and treatment concepts and goals, and ensure Maintain a healthy lifestyle and look for and avoid migraine triggers. Drug treatment is divided into episodic treatment and preventive treatment. 1. Treatment of attacks: Clinical treatment of migraine should usually take medication as soon as symptoms begin. Treatment drugs include non-specific Painkillers such as non-steroidal anti-inflammatory drugs (NSAIDs) and opioids, specific drugs such as wheat Angular preparations and triptans (Table 8-3). Drug selection should be based on comprehensive consideration such as headache severity, accompanying symptoms, and past medication use. Considering, the ladder method and hierarchical drug selection can be used to carry out individualized treatment. Migraine specific treatment drugs Table 8-3 drug Dosage maximum daily dose Half-life (hours) Ergot preparations 1~2 m gPO/SL/PR Ergotamine 2.0 6m gPO/SL/PR Dihydroergotamine 1~2 m gIM;1~3 m gPO 4 m gIM: 9 m gPO 2.5 Triptans sumatriptan 6 mg SC:25~100 m gPO 12 m gSC: 300 m gPO 2.0 naratriptan 2.5m gPO 5 m gPO 5.0~6.3 rizatriptan 5~10 m gPO 30 mg PO 2.0 2.5~5m gP 0 zolmitriptan 10 mg PO 3.0 Almotriptan 6.25~12.5 m gPO 25 m gPO 3.5 Note: PO: oral administration; SL: sublingual administration; PR: rectal administration; IM: intramuscular injection; SC: subcutaneous injection (1) Mild to moderate headache: NSAIDs such as aspirin, n apr oxen, ibuprofen, and double Clofenac (diclofenac) and other effective drugs, if not effective, use specific migraine treatment drugs. Opioids such as pethidine for acute migraine It is also effective for attacks. Because of its carcinogenicity, routine use is not recommended, but for cases where the use of ergot preparations or triptans is contraindicated, such as If there is heart disease, peripheral vascular disease, or migraine during pregnancy, vitiligo treatment can be given to terminate the acute attack of migraine. (2) Moderate to severe headache: For severe attacks, migraine-specific treatment drugs (Table 8-3) can be directly used to improve symptoms as soon as possible. Although some patients have severe headaches but have responded well to NSAIDs in past attacks, NSAIDs can still be used. Ergot preparations are 5- Non-selective agonist of HT 1 receptor, long half-life, low recurrence rate of headache, suitable for patients with long-lasting attacks, triptan It is a 5-HT 1 B/1 D receptor selective agonist. Compound preparations such as ergotamine and caffeine mixture can treat some moderate to severe migraines. Pain attacks. Adverse effects of ergots and triptans include nausea, vomiting, palpitations, irritability, anxiety, peripheral vasoconstriction, and Long-term use of excessive amounts can cause hypertension and ischemic necrosis of limbs. Due to its strong vasoconstriction effect, severe hypertension, heart disease It is contraindicated in sick and pregnant patients. In addition, if ergots and triptans are used too frequently, drug overdose may occur. For headaches, it is recommended to take the medicine no more than 2 to 3 days a week. C GRP receptor antagonists developed in recent years are expected to become safe and effective specific drugs for terminating acute attacks of migraine. (3) Accompanying symptoms: Patients with nausea and vomiting must take antiemetics (such as metoclopramide 10 mg intramuscular injection), and patients with severe vomiting may Give low doses of perphenazine and chlorpromazine. For patients with irritability, benzodiazepines can be given to induce calmness and sleep. 2. Preventive treatment is suitable for: ① Patients with frequent attacks, especially those with more than one attack per week that seriously affect daily life and work. ② Those who are ineffective in acute phase treatment, or unable to undergo acute phase treatment due to side effects and contraindications; ③ may cause permanent neurological deficits Special variant migraine with damage, such as hemiplegic migraine, basilar migraine or migraine infarction. Drug therapy should be a small dose of single drug Start by slowly increasing the dose to the appropriate dose while paying attention to side effects. Preventive treatment can be considered effective if the frequency of migraine attacks is reduced by more than 50%. effect. Effective preventive treatment needs to be continued for about 6 months, after which the dose can be slowly reduced or discontinued. Drugs used clinically for migraine prevention see Table 8-4.